Discussion
It has been reported that hypertrophic cardiomyopathy or dilated cardiomyopathy can cause AS.2,3 Some scholars have proposed the AS is defined by: Atrial electrical activity could not be recorded by routine ECG; The jugular pulse and wave disappeared; The atrial contraction disappeared under X-ray fluoroscopy; QRS wave is the supraventricular pattern; Higher intensity atrial stimulation does not produce atrial excitement.4 Studies have found that atrial muscle degeneration, necrosis, fibrosis, fat cell accumulation and other pathological changes occurred in patients with AS and the changes were mostly irreversible.5 Chhabra L et al. reported that interatrial block will affect atrial electrical and mechanical activity, especially the patients with left atrial enlargement. The atrial injury leads to interatrial block, and finally leads to atrial standstill.6 However, intracardiac electrophysiological examination in AS has not been reported.
In this case, a small amount of potential was observed in the left inferior pulmonary vein, and no electrical activity was measured in other parts of the left atrium, which could indicate AS not caused by interatrial block. AS caused by acute myocarditis has been reported.7 Atrial nonpotential and AS after pericardial effusion have been rarely reported. In this case, rheumatism, tumor, tuberculosis and myocarditis were excluded according to the examination. Pericardial effusion test suggested that inflammatory cells increased, and pericardial effusion decreased after anti-inflammatory treatment. However, the specific mechanism of AS was unknown. The risk of thrombosis and stroke was significantly increased in patients with AS and stroke has been reported in patients with AS,8 so anticoagulation therapy should be actively used in patients with AS. In this case, anticoagulation therapy was performed and there may be other types of arrhythmia in the right atrium during the follow-up.